NF-κB activation and potentiation of proinflammatory responses by the Helicobacter pylori CagA protein

Brandt S, Kwok T, Hartig R, König W, Backert S (2005)


Publication Type: Journal article

Publication year: 2005

Journal

Book Volume: 102

Pages Range: 9300-9305

Journal Issue: 26

DOI: 10.1073/pnas.0409873102

Abstract

The Helicobarter pylori immunodominant protein, CagA, is associated with severe gastritis and carcinoma. Injection of CagA into gastric epithelial cells by type IV secretion leads to actin-cytoskeletal rearrangements and cell scattering. CagA has been reported to have no role in the induction of transcription factor NF-κB and IL-8, which are crucial determinants for chronic inflammation. Here, we provide several lines of evidence showing that CagA is able to induce IL-8 in a time- and strain-dependent manner. We also show that by exchanging specific cagA genes, high IL-8-inducing H. pylori strains could be converted into low inducing strains and vice versa. Our results suggest that IL-8 release induced by CagA occurs via a Ras→Raf→Mek→ Erk→NF-κB signaling pathway in a Shp-2- and c-Met-independent manner. Thus, CagA is a multifunctional protein capable of effecting both actin remodeling and potentiation of chemokine release. © 2005 by The National Academy of Sciences of the USA.

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APA:

Brandt, S., Kwok, T., Hartig, R., König, W., & Backert, S. (2005). NF-κB activation and potentiation of proinflammatory responses by the Helicobacter pylori CagA protein. Proceedings of the National Academy of Sciences of the United States of America, 102(26), 9300-9305. https://doi.org/10.1073/pnas.0409873102

MLA:

Brandt, Sabine, et al. "NF-κB activation and potentiation of proinflammatory responses by the Helicobacter pylori CagA protein." Proceedings of the National Academy of Sciences of the United States of America 102.26 (2005): 9300-9305.

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